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MRCP p1 > nephrology > Flashcards

nephrology Flashcards

1
Q

what nephropathy is HIV associated with?

A

HIV-associated nephropathy (HIVAN) causes collapsing FSGS and usually presents as nephrotic syndrome

. The cause of FSGS in HIV is unclear but may be a result of the virus directly infecting tubular epithelial cells and podocytes.

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2
Q

what are secondary causes of minimal change disease?

A

drugs: NSAIDs, rifampicin
Hodgkin’s lymphoma, thymoma
infectious mononucleosis

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3
Q

what is seen on electron microscopy of minimal change?

A

electron microscopy shows fusion of podocytes and effacement of foot processes

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4
Q

what are the complications of nephrotic syndorme?

A
  • increased risk of thromboembolism related to loss of antithrombin III and plasminogen in the urine: dVT, pulmonary embolism, renal vein thrombosis
  • CKD
  • increased risk of infection - immunogobulin loss
  • hypocalcaemia
  • hyperlipidamaemia
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5
Q

what are the features of fanconi syndorme?

A

reabsorptive disorder of renal tubular transport in teh proximal convoluted tubule:
- type 2 renal tubular acidosis
- polyuria
- aminoaciduria
- glycosuria
- phosphaturia
-osteomalacia

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6
Q

what are the causes of fanconi syndorme?

A

cystinosis (most common cause in children)
Sjogren’s syndrome
multiple myeloma
nephrotic syndrome
Wilson’s disease

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7
Q

what type of bacteira is proetus mirabilis?

A

P. mirabilis is a gram negative, facultatively anaerobic, rod-shaped bacterium which is motile

This organism produces urease which breaks down urea to carbon dioxide and ammonia resulting in a lower pH. The alkaline urine increases the risk of developing struvite stones.

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8
Q

what is used to reduce formation of oxalte stones?

A
  • cholestyramine reduces urinary oxalate secretion
  • pyridoxine reduces urinary oxalate secretion
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9
Q

which chromosome affects ADPKD type 1 and 2?

A

Type 1 - chromsoome 16
type 2 - chromosome 4

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10
Q

how is good pastures/ antiGBM disease diagnsoed?

A

renal biopsy: linear IgG deposits along the basement membrane

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11
Q

what is the tx for anti-GBM disease?

A

plasma exchange (plasmapheresis)
steroids
cyclophosphamide

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12
Q

how do you differentiate between pre-renal uraemia and acute tubular necrosis?

A

urinary sodium

In prerenal uraemia, the kidneys respond to decreased perfusion by conserving sodium, leading to a low urinary sodium concentration (<20 mmol/L). In contrast, ATN is characterised by an inability of the renal tubules to reabsorb sodium properly, resulting in a high urinary sodium concentration (>40 mmol/L)

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13
Q

what are the extra-renal manifestations of ADPKD?

A
  • liver cysts
  • berry aneurysm
  • mitral valve prolapse, mitral/ tricuspid incompetnce
  • cysts in other organs: pancreas, spleen
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14
Q

what are the causes of focal segmental glomerulosclerosis?

A

IHSAS in Arabic mean feeling

I for idiopathic
H for HIV & heroin
S for secondary renal causes IgA nephropathy & reflux nephropathy
A for Alport syndrome
S for Sickle cell

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15
Q

what is the renal biopsy findings of FSGS?

A

renal biopsy:
- focal and segmental sclerosis and hyalinosis on light microscopy
- effacement of foot processes on electron microscopy

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16
Q

MR angiography is now the investigation of choice
how do you differentiate hyperaldosteronism from bilateral renal artery stenosis?

A

both present with high aldosterone levels with hypokalemia

however, renin levels are low in conn’s syndrome. High in renal artery stenosis and barttter syndrome

Aldosterone is elevated in bilateral renal artery stenosis and Bartter syndrome due to reduced renal perfusion. Aldosterone is high in primary hyperaldosteronism due to (most commonly) an aldosterone producing adenoma.

serum renin is usually low in primary hyperaldosteronism due to the resulting hypertension causing excessive renal perfusion, which results in decreased renin production (negative feedback mechanism)

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17
Q

what is the investigation of choice for renal vascular disease?

A

MR angiography is now the investigation of choice

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18
Q

what are the indications of renal replacement therapy?

A

A Acidosis metabolic acidosis
E Electrolytes refractory hyperkalemia or rapidly rising potassium levels
I Ingested substances *
O Overload volume overload refractory to diuresis
U Uremia elevated urea with signs or symptoms of uremia (pericarditis, neuropathy, or uremic encephalopathy)

*Use Mnemonic SLIME for these: salicylates, lithium, isopropanol, methanol, ethylene glycol

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19
Q

what are the criteria to diagnose AKI?

A
  1. Rise in creatinine of 26µmol/L or more in 48 hours OR
  2. > = 50% rise in creatinine over 7 days OR
  3. Fall in urine output to < 0.5ml/kg/hour for more than 6 hours in adults (8 hours in children)

OR

> = 25% fall in eGFR in children / young adults in 7 days.

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20
Q

what is the definition of stage 1 AKI?

A
  • Increase in creatinine to 1.5-1.9 times baseline, or
  • Increase in creatinine by ≥26.5 µmol/L, or
  • Reduction in urine output to <0.5 mL/kg/hour for ≥ 6 hours
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21
Q

what is the definition of stage 2 AKI?

A
  • Increase in creatinine to 2.0 to 2.9 times baseline, or
  • Reduction in urine output to <0.5 mL/kg/hour for ≥12 hours
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22
Q

what is the definition of stage 3 AKI?

A
  • Increase in creatinine to ≥ 3.0 times baseline, or
  • Increase in creatinine to ≥353.6 µmol/L or
  • Reduction in urine output to <0.3 mL/kg/hour for ≥24 hours,

or

The initiation of kidney replacement therapy, or,
In patients <18 years, decrease in eGFR to <35 mL/min/1.73 m2

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23
Q

what are the causes of HAGMA?

A

MUDPILES

Methanol intoxication, Uremia
Diabetic ketoacidosis
Paraldehyde
Isoniazid or Iron overdose, Inborn error of metabolism, Lactic acidosis
Ethylene glycol intoxication Salicylate intoxication

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24
Q

what are the causes of NAGMA??

A

FUSEDCARS

Fistula (biliary, pancreatic), Ureterogastric conduit, Saline administration, Endocrine (Addison disease, hyper-PTH), Diarrhea, Carbonic anhydrase inhibitor, Ammonium chloride, Renal tubular acidosis, Spironolactone

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25
Q

what is the normal anion gap?

A

The normal range = 10-18 mmol/L

26
Q

how does NAGMA happen physiologically?

A

hyperchloraemic metabolic acidosis

27
Q

what is the speciality of urate stones of x-rays?

A

radio-lucent
needs US or CTKUB

28
Q

what are the causes of rapidly progressive glomerulonephritis?

A

Goodpasture’s
ANCA positive vasculitis -granulomatosis with polyangiitis (GPA)

29
Q

what is seen on biopsy of wegner’s glomerulonephritis / granulomatosis with polyangiitis ?

A

glomerular crescents

30
Q

what is the diagnostic features of rhabdomyolysis?

A

acute kidney injury with disproportionately raised creatinine

hyperkalaemia (may develop before renal failure)
metabolic acidosis
high CK

31
Q

what is the mx of nephrogenic diabetes insipidus?

A

thiazides
low salt/protein diet

32
Q

what organism is the highly likely to affect after peritoneal dialysis?

A

Staphylococcus epidermidis

33
Q

what antibodies are found in idiopathic membranous GN?

A

detecting anti-phospholipase A2 antibodies

34
Q

what is the electron microscopy findig of membranous GN?

A

the basement membrane is thickened with subepithelial electron dense deposits. This creates a ‘spike and dome’ appearance

35
Q

what are the causes of membranous GN?

A
  • idiopathic: due to anti-phospholipase A2 antibodies
  • infections: hepatitis B, malaria, syphilis
  • malignancy (in 5-20%): prostate, lung, lymphoma, leukaemia
  • drugs: gold, penicillamine, NSAIDs
  • autoimmune diseases: systemic lupus erythematosus (class V disease), thyroiditis, rheumatoid
36
Q

what is seen on electron microscopy for alport syndrome?

A

characteristic finding is of the longitudinal splitting of the lamina densa of the glomerular basement membrane, resulting in a ‘basket-weave’ appearance

37
Q

why do some pateints fail to respond to erythropoetin therapy?

A

iron deficiency
inadequate dose
concurrent infection/inflammation
hyperparathyroid bone disease
aluminium toxicity

38
Q

what is the hereditary gene link causing nephrogenic diabetes insipidus?

A

Mutations of the AVPR2 (arginine vasopressin receptor 2) gene on the X chromosome are most common, causing a misfolded protein to become trapped within the cell

39
Q

what are the different types of membranoproliferative/ mesangiocapillary glomeruloneprhitis and what are they associated with?

A

Mesangiocapillary glomerulonephritis (membranoproliferative)
type 1: cryoglobulinaemia, hepatitis C
type 2: partial lipodystrophy

40
Q

what monitoring is necessary when putting patients on tacrolimus or ciclosporin?

A

Cardiovascular disease - tacrolimus and ciclosporin can cause hypertension and hyperglycaemia. Tacrolimus can also cause hyperlipidaemia.

Renal failure - due to nephrotoxic effects of tacrolimus and ciclosporin/graft rejection/recurrence of original disease in transplanted kidney

41
Q

what are the features of HSP?

A

-R (rash - palpable purpura , generally below waist)

-O (odema)

-J (joints)

-A Abdominal pain (bowel vascultitis - intussusception )

-K (kidney) nephritis

42
Q

what are the complications of plasma exchange?

A
  • hypocalcaemia: due to the presence of citrate used as an anticoagulant for the extracorporeal system
  • metabolic alkalosis
  • removal of systemic medications
  • coagulation factor depletion
  • immunoglobulin depletion
43
Q

how long does it take for contrast medium to cause nephrotoxicity?

A

Contrast-induced nephropathy occurs 2 -5 days after administration.

44
Q

Differentiating between IgA nephropathy and post-streptococcal glomerulonephritis?

A
  1. post-streptococcal glomerulonephritis is associated with low complement levels
  2. main symptom in post-streptococcal glomerulonephritis is proteinuria (although haematuria can occur)
  3. there is typically an interval between URTI and the onset of renal problems in post-streptococcal glomerulonephritis
45
Q

Dx for Flash pulmonary oedema, U&Es worse on ACE inhibitor?

A

asymmetrical kidneys → renal artery stenosis - do MR angiography

46
Q

what is the chemical also known as struvite?

A

Magnesium ammonium phosphate,

47
Q

what are the endocrine effects of renal cell carcinoma?

A
  1. may secrete erythropoietin (polycythaemia)
  2. parathyroid hormone-related protein (hypercalcaemia), renin
    ACTH
  3. Stauffer syndrome - cholestasis, hepatosplenomegaly - due to increased levels of IL6
48
Q

how does bicalutamide work?

A

blocks the androgen receptor

49
Q

what causes atypical HUS?

A

defect in complement alternative pathway regulation

50
Q

how do you prevent ocntrast-induced nephropathy?

A

intravenous 0.9% sodium chloride at a rate of 1 mL/kg/hour for 12 hours pre- and post- procedure

51
Q

what skin condition are patient on long-term use of immunosuppressants susceptible to?

A

Patients who have received an organ transplant are at risk of skin cancer (particularly squamous cell carcinoma) due to long-term use of immunosuppressants

52
Q

what is the most common cause of Gn in SLE pateints

A

Diffuse proliferative glomerulonephritis is the most common and severe form of renal disease in SLE patients

53
Q

what is seen on biopsy of diffuse proliferatvie GN?

A
  • glomeruli shows endothelial and mesangial proliferation, ‘wire-loop’ appearance
  • if severe, the capillary wall may be thickened secondary to immune complex deposition
  • electron microscopy shows subendothelial immune complex deposits
  • granular appearance on immunofluorescence
54
Q

what are the features of AL amyloidosis?

A

most common form of amylyoidosis

L for immunoglobulin Light chain fragment

due to myeloma, Waldenstrom’s, MGUS

features include: nephrotic syndrome, cardiac and neurological involvement, macroglossia, periorbital eccymoses

55
Q

what are the features of AA amyloidosis?

A

A for precursor serum amyloid A protein, an acute phase reactant

seen in chronic infection/inflammation

e.g. TB, bronchiectasis, rheumatoid arthritis

features: renal involvement most common feature

56
Q

what are the causes of diffuse proliferative glomerlunephritis?

A

post-strep GN
SLE

57
Q

what does renal biopsy show on HSP ?

A

mesangial hypercellularity

58
Q

what is a good prognostic marker in IgA nephropathy?

A

frank haematuria

59
Q

when do you add 5-alpha reductase to alpha blockers in BPH?

A

NICE guidance recommends alpha blocker first line, then adding 5alpha reductase inhibitors if PSA >1.4

60
Q

factors that affect GFR calculations?

A

pregnancy
muscle mass (e.g. amputees, body-builders)
eating red meat 12 hours prior to the sample being taken

MRCP p1 (13 decks)

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